12/28/2022 0 Comments Tremulous behiavior![]() On presentation to the local trauma center, large lacerations were noted on the back of his head. He was combative when found by emergency medical technicians and was given fentanyl, etomidate, and succinylcholine before intubation and sedation in the field. He was the driver and was going 60 miles per hour at the time of the accident. Case ReportĪ 38-year-old man with no known medical history presented to the hospital after being ejected from his vehicle following an accident. In this report, we present a case wherein divalproex sodium, a commercial preparation of valproate, was used successfully in conjunction with other agents to treat a patient with PSH and severe agitation following TBI. Valproate is not mentioned as a potential treatment for PSH-associated agitation despite its use in treatment of agitation in TBI patients. 4 However, literature on the treatment options for PSH-associated agitation is sparse. 2 A variety of medications have been used to address PSH in general including opioids, γ-aminobutyric acid (GABA) agonists, α-agonists, and antipsychotics. 2 There also have been attempts to localize the structural lesions that may lead to PSH with no clear results. Second, normally innocuous sensory inputs trigger strong sympathetic responses. First, there is increased spinal circuit excitation from disconnection of descending inhibitory pathways. 3 In this model, PSH is a 2-step process. One of the more recent theories is the excitatory:inhibitory ratio model. There is still debate about the pathophysiology of PSH as well as its duration. 1 This lack of diagnostic clarity can lead to challenges to treatment, especially when patients present with both PSH and agitation after a new TBI. 2 One symptom that does appear to be missing is agitation, although it has frequently been described as a clinical feature present in PSH. 2 The second part is the Diagnostic Likelihood Tool (DLT), which assesses for features associated with PSH such as an antecedent acquired brain injury, paroxysmal episodes, occurrence 2 weeks after the brain injury, and length of symptoms greater than 3 days. 2 The PSH Assessment Measure (PSH-AM) consists of 2 parts: the first is the Clinical Feature Scale (CFS), which assesses for tachycardia, tachypnea, hypertension, hyperthermia, posturing, and diaphoresis. There have been significant questions raised regarding the diagnostic criteria for PSH, with a consensus process established in 2014. ![]() Its prevalence among TBI patients is debated as well, but estimates range from 7.7% to as high as 33%. 1 While the etiology is debated, it is most commonly associated with traumatic brain injuries (TBIs). Paroxysmal sympathetic hyperactivity (PSH) is a clinical phenomenon characterized by symptoms of sympathetic stimulation such as increased heart rate, blood pressure, temperature, and diaphoresis as well as motor symptoms including agitation, hypertonia, and spasticity. ![]()
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